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首页> 外文期刊>Cellular Physiology and Biochemistry >SUZ12 Depletion Suppresses the Proliferation of Gastric Cancer Cells
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SUZ12 Depletion Suppresses the Proliferation of Gastric Cancer Cells

机译：SUZ12耗竭抑制胃癌细胞的增殖

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biBackground/Aims/i/b SUZ12 and EZH2 are two main components of polycomb repressive complex 2 (PRC2) that is known to be of great importance in tumorigenesis. EZH2 has been reported to play a vital role in pathogenesis of human cancer. However, whether SUZ12 has equivalent roles in tumorigenesis has not been demonstrated. Here, we investigated a possible role of SUZ12 for the proliferation of gastric cancer cells. biMethods/i/b Western-blot analysis was used to detected the levels of SUZ12, H3K27me3, EZH2 and p27 in ten gastric cell lines. SUZ12 was depleted by RNA interference. Cell cycle was detected by flow cytometry. Luciferase assays was to analyze whether miR-200b directly regulate SUZ12. biResults/i/b We found that SUZ12 depletion mediated by RNA interference (RNAi) led to a reduction of gastric cell numbers and arrested the cell cycle at G1/S point. As an important G1/S phase inhibitory gene, p27 is re-induced to some extent by SUZ12 knockdown. Furthermore, we demonstrated that SUZ12 was directly downregulated by miR-200b. biConclusion/i/b We provide evidence suggesting that SUZ12 may be a potential therapeutic target for gastric cancer.
机译：背景/目标 SUZ12和EZH2是聚梳阻抑复合物2（PRC2）的两个主要成分，已知在肿瘤发生中非常重要。据报道，EZH2在人类癌症的发病机理中起着至关重要的作用。但是，尚未证明SUZ12在肿瘤发生中是否具有同等作用。在这里，我们研究了SUZ12在胃癌细胞增殖中的可能作用。 方法 采用Western印迹法检测10种胃癌细胞系中SUZ12，H3K27me3，EZH2和p27的水平。 SUZ12被RNA干扰耗尽。通过流式细胞术检测细胞周期。萤光素酶测定法是分析miR-200b是否直接调节SUZ12。 结果 我们发现，RNA干扰（RNAi）介导的SUZ12耗竭导致胃细胞数量减少，并使细胞周期停留在G1 / S点。作为重要的G1 / S期抑制基因，p27在SUZ12敲除后会在一定程度上被重新诱导。此外，我们证明了miR-200b直接下调了SUZ12。 结论 我们提供的证据表明SUZ12可能是胃癌的潜在治疗靶标。

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